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  1. Article ; Online: Fibronectin: functional character and role in alcoholic liver disease.

    Aziz-Seible, Razia S / Casey, Carol A

    World journal of gastroenterology

    2011  Volume 17, Issue 20, Page(s) 2482–2499

    Abstract: Fibronectins are adhesive glycoproteins that can be found in tissue matrices and circulating in various fluids of the body. The variable composition of fibronectin molecules facilitates a diversity of interactions with cell surface receptors that suggest ...

    Abstract Fibronectins are adhesive glycoproteins that can be found in tissue matrices and circulating in various fluids of the body. The variable composition of fibronectin molecules facilitates a diversity of interactions with cell surface receptors that suggest a role for these proteins beyond the structural considerations of the extracellular matrix. These interactions implicate fibronectin in the regulation of mechanisms that also determine cell behavior and activity. The two major forms, plasma fibronectin (pFn) and cellular fibronectin (cFn), exist as balanced amounts under normal physiological conditions. However, during injury and/or disease, tissue and circulating levels of cFn become disproportionately elevated. The accumulating cFn, in addition to being a consequence of prolonged tissue damage, may in fact stimulate cellular events that promote further damage. In this review, we summarize what is known regarding such interactions between fibronectin and cells that may influence the biological response to injury. We elaborate on the effects of cFn in the liver, specifically under a condition of chronic alcohol-induced injury. Studies have revealed that chronic alcohol consumption stimulates excess production of cFn by sinusoidal endothelial cells and hepatic stellate cells while impairing its clearance by other cell types resulting in the build up of this glycoprotein throughout the liver and its consequent increased availability to influence cellular activity that could promote the development of alcoholic liver disease. We describe recent findings by our laboratory that support a plausible role for cFn in the promotion of liver injury under a condition of chronic alcohol abuse and the implications of cFn stimulation on the pathogenesis of alcoholic liver disease. These findings suggest an effect of cFn in regulating cell behavior in the alcohol-injured liver that is worth further characterizing not only to gain a more comprehensive understanding of the role this reactive glycoprotein plays in the progression of injury but also for the insight further studies could provide towards the development of novel therapies for alcoholic liver disease.
    MeSH term(s) Disease Progression ; Extracellular Matrix/physiology ; Fibronectins/physiology ; Hepatic Stellate Cells/physiology ; Humans ; Liver Diseases, Alcoholic/physiopathology
    Chemical Substances Fibronectins
    Language English
    Publishing date 2011-04-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2185929-2
    ISSN 2219-2840 ; 1007-9327
    ISSN (online) 2219-2840
    ISSN 1007-9327
    DOI 10.3748/wjg.v17.i20.2482
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Fibronectin

    Razia S Aziz-Seible / Carol A Casey

    World Journal of Gastroenterology, Vol 17, Iss 20, Pp 2482-

    Functional character and role in alcoholic liver disease

    2011  Volume 2499

    Abstract: Fibronectins are adhesive glycoproteins that can be found in tissue matrices and circulating in various fluids of the body. The variable composition of fibronectin molecules facilitates a diversity of interactions with cell surface receptors that suggest ...

    Abstract Fibronectins are adhesive glycoproteins that can be found in tissue matrices and circulating in various fluids of the body. The variable composition of fibronectin molecules facilitates a diversity of interactions with cell surface receptors that suggest a role for these proteins beyond the structural considerations of the extracellular matrix. These interactions implicate fibronectin in the regulation of mechanisms that also determine cell behavior and activity. The two major forms, plasma fibronectin (pFn) and cellular fibronectin (cFn), exist as balanced amounts under normal physiological conditions. However, during injury and/or disease, tissue and circulating levels of cFn become disproportionately elevated. The accumulating cFn, in addition to being a consequence of prolonged tissue damage, may in fact stimulate cellular events that promote further damage. In this review, we summarize what is known regarding such interactions between fibronectin and cells that may influence the biological response to injury. We elaborate on the effects of cFn in the liver, specifically under a condition of chronic alcohol-induced injury. Studies have revealed that chronic alcohol consumption stimulates excess production of cFn by sinusoidal endothelial cells and hepatic stellate cells while impairing its clearance by other cell types resulting in the build up of this glycoprotein throughout the liver and its consequent increased availability to influence cellular activity that could promote the development of alcoholic liver disease. We describe recent findings by our laboratory that support a plausible role for cFn in the promotion of liver injury under a condition of chronic alcohol abuse and the implications of cFn stimulation on the pathogenesis of alcoholic liver disease. These findings suggest an effect of cFn in regulating cell behavior in the alcohol-injured liver that is worth further characterizing not only to gain a more comprehensive understanding of the role this reactive glycoprotein plays in the progression of injury but also for the insight further studies could provide towards the development of novel therapies for alcoholic liver disease.
    Keywords Fibronectin ; Liver disease ; Alcoholic liver disease ; Endocytosis ; Cellular fibronectin ; Diseases of the digestive system. Gastroenterology ; RC799-869 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Gastroenterology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Subject code 610
    Language English
    Publishing date 2011-01-01T00:00:00Z
    Publisher Baishideng Publishing Group Co., Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Cellular fibronectin stimulates hepatocytes to produce factors that promote alcohol-induced liver injury.

    Aziz-Seible, Razia S / McVicker, Benita L / Kharbanda, Kusum K / Casey, Carol A

    World journal of hepatology

    2011  Volume 3, Issue 2, Page(s) 45–55

    Abstract: Aim: To examine the consequences of cellular fibronectin (cFn) accumulation during alcohol-induced injury, and investigate whether increased cFn could have an effect on hepatocytes (HCs) by producing factors that could contribute to alcohol-induced ... ...

    Abstract Aim: To examine the consequences of cellular fibronectin (cFn) accumulation during alcohol-induced injury, and investigate whether increased cFn could have an effect on hepatocytes (HCs) by producing factors that could contribute to alcohol-induced liver injury.
    Methods: HCs were isolated from rats fed a control or ethanol liquid diet for four to six weeks. Exogenous cFn (up to 7.5 μg/mL) was added to cells cultured for 20 h, and viability (lactate dehydrogenase,LDH), apoptosis (caspase activity) and secretion of proinflammatory cytokines (tumor necrosis factor alpha, TNF-α and interleukin 6 IL-6), matrix metalloproteinases (MMPs) and their inhibitors (tissue inhibitors of metalloproteinases, TIMPs) was determined. Degradation of iodinated cFn was determined over a 3 h time period in the preparations.
    Results: cFn degradation is impaired in HCs isolated from ethanol-fed animals, leading to its accumulation in the matrix. Addition of exogenous cFn did not affect viability of HCs from control or ethanol-fed animals, and apoptosis was affected only at the higher concentration. Secretion of MMPs, TIMPs, TNF-α and IL-6, however, was increased by exogenously added cFn, with HCs from ethanol-fed animals showing increased susceptibility compared to the controls.
    Conclusion: These results suggest that the elevated amounts of cFn observed in alcoholic liver injury can stimulate hepatocytes to produce factors which promote further tissue damage.
    Language English
    Publishing date 2011-03-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2573703-X
    ISSN 1948-5182 ; 1948-5182
    ISSN (online) 1948-5182
    ISSN 1948-5182
    DOI 10.4254/wjh.v3.i2.45
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Cellular fibronectin stimulates hepatocytes to produce factors that promote alcohol-induced liver injury

    Razia S Aziz-Seible / Benita L McVicker / Kusum K Kharbanda / Carol A Casey

    World Journal of Hepatology, Vol 3, Iss 2, Pp 45-

    2011  Volume 55

    Abstract: AIM: To examine the consequences of cellular fibronectin (cFn) accumulation during alcohol-induced injury, and investigate whether increased cFn could have an effect on hepatocytes (HCs) by producing factors that could contribute to alcohol-induced liver ...

    Abstract AIM: To examine the consequences of cellular fibronectin (cFn) accumulation during alcohol-induced injury, and investigate whether increased cFn could have an effect on hepatocytes (HCs) by producing factors that could contribute to alcohol-induced liver injury.METHODS: HCs were isolated from rats fed a control or ethanol liquid diet for four to six weeks. Exogenous cFn (up to 7.5 μg/mL) was added to cells cultured for 20 h, and viability (lactate dehydrogenase,LDH), apoptosis (caspase activity) and secretion of proinflammatory cytokines (tumor necrosis factor alpha, TNF-α and interleukin 6 IL-6), matrix metalloproteinases (MMPs) and their inhibitors (tissue inhibitors of metalloproteinases, TIMPs) was determined. Degradation of iodinated cFn was determined over a 3 h time period in the preparations.RESULTS: cFn degradation is impaired in HCs isolated from ethanol-fed animals, leading to its accumulation in the matrix. Addition of exogenous cFn did not affect viability of HCs from control or ethanol-fed animals, and apoptosis was affected only at the higher concentration. Secretion of MMPs, TIMPs, TNF-α and IL-6, however, was increased by exogenously added cFn, with HCs from ethanol-fed animals showing increased susceptibility compared to the controls.CONCLUSION: These results suggest that the elevated amounts of cFn observed in alcoholic liver injury can stimulate hepatocytes to produce factors which promote further tissue damage.
    Keywords Alcoholic liver diseases ; Hepatocytes ; Fibronectin ; Asialoglycoprotein receptor ; Inflammation ; Fibrosis ; Diseases of the digestive system. Gastroenterology ; RC799-869 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Gastroenterology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Subject code 610
    Language English
    Publishing date 2011-02-01T00:00:00Z
    Publisher Baishideng Publishing
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

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  5. Article ; Online: Ethanol feeding potentiates the pro-inflammatory response of Kupffer cells to cellular fibronectin.

    Aziz-Seible, Razia S / Lee, Serene M / Kharbanda, Kusum K / McVicker, Benita L / Casey, Carol A

    Alcoholism, clinical and experimental research

    2011  Volume 35, Issue 4, Page(s) 717–725

    Abstract: Background: Excessive alcohol consumption leads to the increased extracellular matrix deposition of cellular fibronectin (cFn) in the liver, which is also implicated as an initiating event in the fibrogenic process. We propose that cFn directly ... ...

    Abstract Background: Excessive alcohol consumption leads to the increased extracellular matrix deposition of cellular fibronectin (cFn) in the liver, which is also implicated as an initiating event in the fibrogenic process. We propose that cFn directly stimulates Kupffer cells (KCs), which are involved in the early response to tissue damage, to produce factors that enhance the progression of alcohol-induced liver injury toward inflammation and fibrosis.
    Method: KCs were isolated from rats fed a control or ethanol liquid diet for 4 to 6 weeks. The effect of exogenous cFn on KC viability and the secretion of the cytokines, TNF-α and IL-6, as well as of matrix remodeling factors, MMP-2 and TIMP-2, was determined after 20 hours of cell culture.
    Results: For KCs from both control- and ethanol-fed rats, viability remained unaffected by treatment with cFn. TNF-α and IL-6 production were increased in KCs exposed to cFn, with cells treated with 1, 2.5, and 5 μg/ml cFn secreting significantly higher levels of both cytokines compared with untreated cells (p < 0.05). Chronic ethanol administration resulted in a significantly enhanced secretion of IL-6 by KCs regardless of treatment with cFn. When MMP-2 protein and activity levels were measured by western blot analysis and gelatin zymography, respectively, we found that cFn stimulated a dramatic increase in both cells from ethanol- and control-fed rats, with the KCs from ethanol animals being more responsive to cFn at higher concentrations (p < 0.05). Significantly higher levels of TIMP-2, which inhibits both the activation and activity of MMP-2, were secreted by KCs treated with 5 μg/ml cFn. Correspondingly, more pro-MMP-2 than active-MMP-2 was detected.
    Conclusion: Altogether, these results show that cFn stimulates KCs to produce factors that may enhance the promotion of tissue damage and that ethanol administration increases these responses.
    MeSH term(s) Animals ; Caspase 3/metabolism ; Cell Culture Techniques ; Cell Survival/drug effects ; Central Nervous System Depressants/metabolism ; Central Nervous System Depressants/pharmacology ; Central Nervous System Depressants/toxicity ; Ethanol/metabolism ; Ethanol/pharmacology ; Ethanol/toxicity ; Extracellular Matrix/physiology ; Fibronectins/physiology ; Inflammation/chemically induced ; Inflammation/physiopathology ; Interleukin-6/metabolism ; Kupffer Cells/cytology ; Kupffer Cells/drug effects ; Kupffer Cells/pathology ; Kupffer Cells/physiology ; Liver/cytology ; Liver/physiopathology ; Male ; Matrix Metalloproteinase 2 ; Rats ; Rats, Wistar ; Tissue Inhibitor of Metalloproteinase-2/metabolism ; Tumor Necrosis Factor-alpha
    Chemical Substances Central Nervous System Depressants ; Fibronectins ; Interleukin-6 ; Tumor Necrosis Factor-alpha ; Tissue Inhibitor of Metalloproteinase-2 (127497-59-0) ; Ethanol (3K9958V90M) ; Caspase 3 (EC 3.4.22.-) ; Matrix Metalloproteinase 2 (EC 3.4.24.24)
    Language English
    Publishing date 2011-01-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 428999-7
    ISSN 1530-0277 ; 0145-6008
    ISSN (online) 1530-0277
    ISSN 0145-6008
    DOI 10.1111/j.1530-0277.2010.01389.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1375: Show issues Location:
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